A Case of Kaposi’s Sarcoma during Primary HIV-1 Infection

Abstract

The majority of cases of Kaposi’s sarcoma (KS) occur at low CD4 counts during chronic HIV-1 infection. We present a case of KS which was diagnosed during primary HIV-1 infection. This report aims to draw attention that KS may occur early in the course of HIV-1 infection and that primary HIV-1 infection may rapidly progress to AIDS.

Introduction

Kaposi’s sarcoma (KS) is a low-grade vascular tumor caused by human herpesvirus 8 (HHV8). ¹ It is one of the most common neoplasms in HIV-1-infected individuals. With the introduction of combination antiretroviral therapy (cART), the incidence of KS has decreased significantly. ² Traditionally, a low CD4 count during chronic HIV-1 infection was the most important factor associated with the development of KS, although recent studies have shown that the majority of KS now occurs at higher CD4 counts. ^3,4 We report a patient who presented with KS during primary HIV-1 infection (PHI).

Case Report

A 48-year-old homosexual man was diagnosed with PHI in June 2009, based on an indeterminate Western blot (p24 and gp120/160 antibodies were detected), and a plasma viral load (pVL) of 267.479 copies/mL. Three weeks prior to the diagnosis, the patient had experienced symptoms which were compatible with an acute retroviral syndrome: fever, sore throat, a dry cough, myalgia, fatigue, and weight loss of 5 kg. Physical examination revealed no abnormalities. Laboratory investigations showed a mild anemia, thrombocytopenia, and elevated liver enzymes. The CD4 count was 210 cells/mm³, CD8 2310 cells/mm³, and CD4/8 ratio 0.09. No transmitted drug resistance mutations were present and the HIV-1 strain belonged to subtype B. Using MT-2 assay to define HIV-1 tropism, no CXCR4-tropic virus was detected. Hepatitis B/C and syphilis serology were negative.

Eleven weeks after HIV diagnosis, the patient discovered a small purple-brown lesion on his left forearm which was a clinical suspect for KS (Figure 1). The diagnosis was confirmed with a skin biopsy. The CD4 count had increased to 500 cells/mm³ and the pVL had dropped significantly to 64.218 copies/mL. The HHV8 load ⁵ was 799 copies/mL. Retrospectively, sequential HHV8 loads were performed on stored plasma samples and HHV8 load at the time of PHI diagnosis was 163 copies/mL (Figure 2). Other possible underlying diseases like Castleman disease, another HHV8-related disease, were excluded.

Figure 1.

Kaposi’s sarcoma on the forearm of the patient

Figure 2.

CD4 count, HIV-1 RNA, and HHV8 DNA in sequential plasma samples from the time of HIV-1 diagnosis. cART indicates combination antiretroviral therapy; HHV8, human herpesvirus 8; KS, Kaposi’s sarcoma; PHI, primary HIV-1 infection. The filled symbols denote undetectable plasma HIV-1 RNA or HHV8 DNA.

Since the patient was recently diagnosed with PHI and was recovering from the PHI-associated transient low CD4 count and peak pVL, we decided to defer cART to await spontaneous regression. During the following months, the KS lesion on the arm remained stable and no new lesions occurred. Thirty-six weeks after HIV diagnosis, the CD4 count had dropped to 310 cells/mm³, the pVL was 18. 138 copies/mL, and the HHV8 load had increased to 10.600 copies/mL (Figure 2). cART was initiated. The patient responded well to the therapy. Within 8 weeks, HIV-1 viral suppression in plasma was achieved, CD4 count increased to 430 cells/mm³, and plasma HHV8 became undetectable. The KS lesion disappeared within the following 6 months.

Discussion

The natural history of HIV-1 infection varies widely between patients and may be affected by viral and/or host factors. Rapid progression to AIDS shortly after PHI has been described previously, ^6,7 including a case of KS diagnosed 24 months after PHI. ⁸ Our patient was symptomatic during PHI, which is a strong predictor of AIDS progression. ⁹ To our knowledge, this is the first patient in whom KS was diagnosed during PHI.

Unfortunately, we were not able to determine the immunoglobulin (Ig) M and IgG antibody titers against HHV8 to distinguish between an acute HHV8 infection or a reactivation of an existing HHV8 infection. Since the patient had a transient immunosuppression and a peak pVL as a result of PHI, reactivation of KS seems likely caused by the immunodeficiency itself and/or by direct effects of HIV-1. ¹

This case demonstrates that KS may occur early in the course of HIV-1 infection and that symptomatic PHI may rapidly progress to AIDS.